Incidence
• The most common structural cause of
urinary outflow obstruction in pediatric
practice
• The most common type of obstructive
uropathy leading to childhood renal failure
• 1 of every 5000 to 8000 male births
• 10% of prenatally diagnosed
hydronephrosis
• 1 PUV in 1250 fetal ultrasound
I. RENAL DYSPLASIA
II. RENAL FUNCTION
III. RENAL TUBULAR FUNCTION
IV. HYDRONEPHROSIS
V. VUR
VI. VESICAL DYSFUNCTION
VII. VALVE BLADDER
1-Renal Dysplassia
• Defined as a congenital defect of tissue
development without premalignant potential
• Histological diagnosis
• Cause ?
1- high pelvic pressure during
nephrogenesis
2- primary embryologic abnormality
from abnormal position of uteteric bud
2-Renal Function
• Children with PUV may demonstrate
gradual loss of renal function over time
• Cause:
1- Renal parenchymal dysplasia
2- Incomplete relief of obstruction
3-parenchymal injury from :
* UTI
*HTN
*Progressive glomerulosclerosis
from hyperfiltration
* Obstruction
• ESRD
-Occurs in 25% - 40%
-1/3 soon after birth
-2/3 during late teenager
3-Renal Tubular Function
• 50% of patients with PUV have impairment
concentration ability
• Persistently high urinary flow rate
regardless of fluid intake or state of
hydration
• severe dehydration and electrolyte
imbalance
• ureteral dilatation and high resting vesical
pressure
4-Hydronephrosis
• Significant urethral obstruction variable
degree of ureteral dilatation
• After relief of obstruction : gradual but
substantial reduction of hydronephrosis
• If not reduced we have to role out:
1- High intravesical pressure
2- ureteral muscle weakness
3- UVJ obstruction
6-Vesical Dysfunction
• Commonly presented in patient with PUV
• Usually primary secondary to irreversible
change in organization and function of the
smooth muscle from outlet obstruction
• Present as as urinary incontinence (20%)
• Bladder dysfunction persist in 75 % after valve
ablation
• May cause deterioration of renal function
• Three groups of dysfunction were described
- Detrusor –hyperreflexia (29%)
- Hypertonic and poor compliant bladder
(31%)
- Myogenic failure and overflow
incontinence (40%)
7-VALVE BLADDER
• Even after relief of obstruction a significant
number of patient will continue to have
hpertonia and detrusor hyperreflexia and
low compliance
• Physiological obstruction of the ureter
associated with bladder filling
• persistence hydronephrosis and/or
urinary incontinence
PROGNOSTIC FACTOR
Good Factors
• Nadir creatinine < 0.8 mg/dl
• S. creatinine < 1 mg/dl
• Pop-off mechanism
- VURD
- Ascitis
- Large bladder diverticulum
Bad Factors
• Age
• Delayed correction
• GFR < 50 % of normal in infancy
• VUR
- Bil -----> 57 % mortality
- Uni. -----> 17 %
- Non -----> 9 %
• Loss of cortico medullary junction
• delayed incontinence beyond 5 years
Clinical presentation
• Variable
• Age dependent
= Prenatally : 70% of PUV by ltrasound
= Newborn: - Abdominal mass
- Ascites
- Respiratory distress
- Urosepsis
- Delayed viding or poor stream
Prenatal Ultrasound
• Change the the incidence of PUV
• Prepare physician for immediate postnatal
management
• Finding: -bilateral hydroureteronephrosis
-distended, thick wall bladder
-+/- oligohydramnios
• The earlier PUV detected the poorer the
diagnosis
Postnatal Ultrasound
• To evaluate the effect of PUV on the urinary
tract rather than to diagnose PUV
• Typical finding: wide prostatic urethra,thick-
walled bladder,and upper tract dilatation
• Assessment of renal parenchyma
• VUR in 50% of patients with PUV
• Normal MCUG exclude PUV
Functional assessment
• Diuretic Radioisotope Scan
- DTPA OR MAG-3
- with urethral catheter in place
-Exclude obstruction and assess split
renal function
• Serum Creatinine
-Immediately after birth reflect maternal
createnin